The “ ” ( ) transcript NF - ĸB interacting long noncoding RNA NKILA is antisense to cancer - associated gene PMEPA

This correspondence concerns a recent publication in by Liu et al. Cancer Cell who analyzed a long noncoding RNA (lncRNA) that they designated “ ”. NKILA Liu et al. found that (1) is upregulated by immunostimulants, (2) has a NKILA promoter with an NF-ĸB binding motif, (3) can bind to the p65 protein of the NF-ĸB transcription factor and then interfere with phosphorylation of IĸBα, and (4) negatively affects functions that involve NF-ĸB pathways. And, importantly, they found that (5) low expression in breast cancers is associated with NKILA poor patient prognosis. However, they entirely failed to mention , a PMEPA1 gene which runs antisense to , and the expression of which is associated NKILA with several tumors and which encodes a protein that participates in immune pathways. The locus, including its promoter region, which Liu et al. only discuss PMEPA1 in regard to , is highly conserved through evolution. Our impression is NKILA that emerged only later in evolution, possibly as an additional means of NKILA regulation. Liu et al., however, only consider direct binding between PMEPA1 and NF-ĸB as the mechanism for their observations of NKILA in vivo NKILA function, but do not provide solid evidence for their model. If in vivo observations by Liu et al. could be explained by regulation of , NKILA PMEPA1 it would contribute to the establishment of as an important topic of PMEPA1 cancer research. We feel that the herein presented discussion is necessary for a correct interpretation of the Liu et al. article. Johannes M. Dijkstra ( ) Corresponding author: [email protected] Dijkstra JM and Alexander DB. How to cite this article: The “ ” ( ) transcript is antisense to NF-ĸ B interacting long noncoding RNA NKILA 2015, :96 (doi: ) cancer-associated gene [version 1; referees: 2 approved] PMEPA1 F1000Research 4 10.12688/f1000research.6400.1 © 2015 Dijkstra JM and Alexander DB. This is an open access article distributed under the terms of the Copyright: Creative Commons Attribution , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Data associated Licence with the article are available under the terms of the (CC0 1.0 Public domain dedication). Creative Commons Zero "No rights reserved" data waiver The author(s) declared that no grants were involved in supporting this work. Grant information: Competing interests: No competing interests were disclosed. 22 Apr 2015, :96 (doi: ) First published: 4 10.12688/f1000research.6400.1 1